INTRODUCTION

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A virulent strain of Haemophilus influenzae type b was used to construct a lambda library of chromosomal DNA in Charon 4, amplified in Escherichia coli. From this library a recombinant (I-69) phage was isolated that contained a 10.2-kilobase-pair fragment of DNA eliciting H. influenzae transformants whose colonies had a distinctive opaque phenotype. Compared with their H. influenzae parent strains the opaque I-69 transformants had two defined cell wall alterations: one in the lipopolysaccharide (greater mobility on sodium dodecyl sulfate-polyacrylamide gel electrophoresis) and one in the outer membrane proteins. The I-69 transformant of virulent type b strain Rd-/b+ had stable expression of type b capsule. In contrast to strain Rd-/b+, the Rd-/b+/I-69 transformant was serum sensitive in vitro and avirulent in vivo in rats. Thus the potential of H. influenzae type b organisms to cause invasive infection can be substantially attenuated by altering the expression of one or more genes that affect the cell wall composition.

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A local defense mechanism in bacterial meningitis was evaluated in humans by measuring complement-mediated opsonic activity (CMOA) in normal and infected cerebrospinal fluid (CSF) with a complement-dependent phagocytic bactericidal assay. CMOA was absent in normal untreated CSF and remained undetectable in 20 samples of CSF from patients with viral meningitis and five samples from patients with acute meningococcemia. In contrast, 15 of 27 samples of CSF from patients with acute bacterial meningitis had a measurable CMOA, which was correlated with protein concentrations (P< 0.01) and C4 hemolytic activity (P< 0.001) in the CSF. A favorable outcome of bacterial meningitis was associated with the presence of CMOA in CSF (P < 0.005). Recovery was also correlated with higher levels of C4 (P < 0.01) and C3 (P < 0.05) in CSF and with lower concentrations of microorganisms in the sample of CSF collected at the time of admission (P< 0.01). Thus, CMOA, although absent in normal CSF, can appear in CSF during acute bacterial meningitis, particularly in patients who recover completely.Mortality and morbidity from acute bacterial meningitis are still high despite substantial progress in diagnosis and treatment [1][2][3]. The development and course of meningeal infection are governed by the complex interaction of many variables [4], including (1) microbial virulence factors such as encapsulation [5,6], (2) clearance of bacteria from the blood [7][8][9], (3) antibacterial mechanisms in the subarachnoid space [10], (4) anatomic and functional changes resulting from inflammation [11,12], and (5) antibiotic therapy. Because bacterial meningitis is in essence a closed-